GI - Liver failure Flashcards
(7) Key Functions of the Liver
- Synthesis of clotting factors (except factor 8)
- Glucose homeostasis-gluconeogenesis, glycogen storage
- Albumin synthesis
- Conjugation and clearance of bilirubin
- NH3 metabolism- the urea cycle
- Drug metabolism and clearance
- Immune - dealing with gut derived bacteria and bacterial products
What (3) can you check for routine liver function tests?
- bilirubin
- albumin
- clotting profile
Which clotting profile tells you more about liver disease?
INR affected more by liver disease than APTT
Why may cholestasis lead to higher INR?
Due to poor absorption of fat soluble vitamins including vitamin K -> vitamin K deficiency -> reduced factors 2, 7, 9, 10 -> higher INR
45yo female, 7 wks post total abdominal hysterectomy •Increasing abdominal pain over 2 days •Vomiting •No bowel actions •Anorexia •Weight loss (10kg over last 7 weeks) taking Paracetamol PRN, Mylanta PRN
Soft non-tender, distended abdomen
AXR - incomplete mid to distal small bowel obstruction
Dx?
Recurrent subacute bowel obstruction secondary to adhesions from previous TAH
Initial Mx of bowel obstruction
–Nasogastric tube
–Intravenous therapy and electrolyte replacement
–NBM
–Analgesia (paracetamol 1g QID strict)
(4) common causes of acute liver injury
- Drug poisoning: paracetamol
- Acute viral hepatitis: hepatitis A, hepatitis B, hepatitis C. Less common EBV, others
- Idiosyncratic acute drug reactions
- Ischaemia: Circulatory shock, acute severe heart failure
Ix for acute liver injury
- paracetamol in blood
- HCV Ab
- IgM anti-HAV, IgG anti-HAV
- HBsAg, HBcAg, HBsAb
- Liver ultrasound
What do HBsAg, HBcAg, HBsAb tell you?
HBsAg: RECENT infection or vaccination
HBcAg: previous/current INFECTION ONLY with HepB
HBsAb: previous/current infection OR vaccination
What (7) are the common causes of acute hepatitis ?
1) Acute viral hepatitis
2) Drug related
3) Ischaemic hepatitis
4) Autoimmune
5) Acute Budd Chiari
6) Wilson’s disease
7) idiopathic
When (3 criteria) do you transfer patient to a liver transplant unit due to acute liver injury?
–INR > 1.5 and rising (except POD)
–Any encephalopathy
–Poor prognosis
What may Ingestion of 10 or more standard paracetamol tablets result in?
fulminant hepatic failure resulting in death within 5-7 days if unchecked
Define acute liver failure
- Rapid deterioration of liver function in previously normal liver
- Trey and Davidson 1970 : “jaundice to encephalopathy within 1.5, any encephalopathy, duration of illness (jaundice) up to 26 weeks
Intervention for paracetamol acute liver failure
- when is it effective
- mechanism
NAC (N-acetylcysteine)
100% effective if given within 8 hours of ingestion, regardless of dose ingested
–Acts as glutathione donor
–Reduces production of toxic metabolite (NAPQI)
Intervention for hep B acute liver failure
Antivirals
Intervention for Wilson’s acute liver failure
Chelation/Exchange
Intervention for Budd Chiari acute liver failure
TIPS (transjugular intrahepatic portosystemic shunts)
I.e. shunt connecting hepatic vein with portal vein to allow portosystemic communication
What is Budd Chiari syndrome? What is the classical triad of symptoms
a condition caused by occlusion of the hepatic veins (e.g. clot) that drain the liver.
Classical triad Px:
- abdominal pain
- ascites
- liver enlargement.
Describe primary & secondary Budd-Chiari syndrome and their common causes
Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein
Related with:
- Polycythemia vera
- Pregnancy
- Postpartum state
- OCP
- Paroxysmal nocturnal haemoglobinuria
- Hepatocellular carcinoma
- Lupus anticoagulants
Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)
Intervention for Autoimmune acute liver failure
Steroids
(3) roles for liver biopsy in acute liver failure
- Quantify extent of liver injury
- Establish aetiology
- Guide to treatment
What criteria do you use to choose patients for liver transplantation?
King’s college criteria
For identifying patients with poor prognosis who need transplantation
What is the toxic dose of paracetamol?
- 24 hours
- 48 hours
- > 48 hours
- 24 hours – 200mg/kg or 10g - whichever is less
- 48 hours – 150 mg/kg or 6g per day – whichever is less
- > 48 hours – 100 mg/kg or 4g per day – whichever is less
(2) common clinical scenarios of paracetamol OD fulminant hepatic failure
- Prolonged courses in fasting individuals: therapeutic doses
- Supra-therapeutic doses in alcoholics & often in short courses
How does paracetamol metabolism occur in the liver?
95% of paracetamol is bound by glucuronide & excreted in bile
5% are metabolised by P450 to NAPQI. Some of them are conjugated with glutathione & hence non toxic.
But when both glucuronide & glutathione are used up, the unconjugated NAPQI cause hepatotoxicity.
General Mx for paracetamol OD acute liver injury
- prevention of absorption
- symptomatic care
- risk assessment
- specific care
•Prevention of absorption
–Activated charcoal within 60 minutes of ingestion
•Symptomatic care
–Anti-emetics
•Risk assessment
–Dose based / plasma paracetamol concentration
•Specific care
–N-acetylcysteine
Describe the use of activated charcoal & its SE
Used to treat poisonings and overdoses following oral ingestion.
- not effective for a number of poisonings including strong acids or alkali, cyanide, iron, lithium, arsenic, methanol, ethanol or ethylene glycol
- over-the-counter drug to treat diarrhea, indigestion, and flatulence.
SE:
- pulmonary aspiration which can sometimes be fatal if immediate medical treatment is not initiated.
- contraindicated when the ingested substance is an acid, an alkali, or a petroleum product.
Describe the Mx of paracetamol OD for:
- 8 hours
measure serum paracetamol level
1-8hours:
- measure serum paracetamol level -> plot serum paracetamol level on nomogram, if over nomogram treatment line -> NAC infusion
> 8 hours:
- commence NAC infusion -> measure serum paracetamol level & ALT. Plot serum paracetamol level on nomogram, if over nomogram treatment line, continue NAC infusion till normalised ALT.
Causes of chronic liver disease (the rule of 3/s)
- Most common: Alcohol, HBV, HCV
- Genetic: Wilson’s disease, Haemochromatosis, A1AT deficiency
- Auto-immune: Primary biliary cirrhosis, primary sclerosing cholangitis, Autoimmune hepatitis
- Other: NASH, drugs, budd chiari syndrome
(3) genetic causes of chronic liver disease
- Wilson’s disease
- Haemochromatosis
- A1AT deficiency
(3) autoimmune causes of chronic liver disease
- Primary biliary cirrhosis
- primary sclerosing cholangitis
- Autoimmune hepatitis
(3) most common causes of chronic liver disease
Alcohol, HBV, HCV
Ix for chronic liver disease to define the aetiology
- HCV Ab
- HBsAg, HBcAb, HBsAb
- Caeruloplasmin (low in Wilson’s disease)
- A1AT
- Fe studies (haemochromatosis)
- ANA, SMA, AMA (autoimmune)
(3) Cx of chronic liver failure & hence preventive Mx
- Hepatoma (patient needs screening)
- Variceal bleeding (patient needs screening)
- Ascites (needs prophylacic antibiotics)
